A model is proposed to explain the releasing action of amphetamine. In this model, the neuronal uptake of amphetamine as well as biogenic amines is carrier mediated. Upon entering the neuron, amphetamine displaces biogenic amines from storage vesicles. The displaced amine binds to the carrier, which is now on the inside of the membrane, and the amine is transported out of the nerve ending. This binding to the carrier protects the displaced amine from deamination by intraneuronal monoamine oxidase. Fenfluramine, a lipid soluble analogue of amphetamine, enters the neuron by passive diffusion and the displaced biogenic amine is metabolized by intraneuronal monoamine oxidase since insufficient carrier is available on the inside of the membrane. This model will be examined by isolating norepinephrine and dopamine enriched synaptosomes, and characterizing the uptake and accumulation of 3H-amphetamine and 3H-analogues of amphetamine. In the model, sodium ion is cotransported with biogenic amines. Thus sodium ion concentrations inside and outside of the nerve ending will be altered and the resultant changes in the uptake of amphetamine and amphetamine analogues will be studied. Storage vesicles from synaptosomes will be isolated and the ability of amphetamine analogues to displace endogenous norepinephrine and dopamine will be measured. Finally, the efflux of unbound norepinephrine and dopamine produced by amphetamine analogues will be characterized.